Immacolata A. Cazzato
The Catholic University of America
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Immacolata A. Cazzato.
Alimentary Pharmacology & Therapeutics | 2004
E.C. Nista; Marcello Candelli; Filippo Cremonini; Immacolata A. Cazzato; M.A. Zocco; Francesco Franceschi; Giovanni Cammarota; Giovanni Gasbarrini; Antonio Gasbarrini
Background : Helicobacter pylori eradication fails in about 10% of patients, particularly because of the occurrence of resistance to antibiotics and side‐effects. During anti‐H. pylori therapy, probiotics have been successfully used to reduce the incidence of side‐effects.
Alimentary Pharmacology & Therapeutics | 2002
Alessandro Armuzzi; Marcello Candelli; M.A. Zocco; A. Andreoli; A. De Lorenzo; E.C. Nista; Luca Miele; Filippo Cremonini; Immacolata A. Cazzato; Antonio Grieco; Giovanni Gasbarrini; Antonio Gasbarrini
Carbon‐labelled breath tests were proposed as tools for the evaluation of human liver function 30 years ago, but have never become part of clinical routine. One reason for this is the complex role of the liver in metabolic regulation, making it difficult to provide essential information for the management of patients with liver disease with a single test and to satisfy the hepatology community. As a result, a battery of breath tests have been developed. Depending on the test compound administered, different metabolic pathways (microsomal, cytosolic, mitochondrial) can be examined. Most available data come from microsomal function tests, whilst information about cytosolic and mitochondrial liver function is more limited. However, breath tests have shown promise in some studies, in particular to predict the outcome of patients with chronic liver disease or to monitor hepatic function after treatment. Whilst we await new substrates that can be used to measure liver function in a more valid manner, and large prospective studies to assess the usefulness of available test compounds, the aim of this review is to describe how far we have come in this controversial and unresolved issue.
Alimentary Pharmacology & Therapeutics | 2003
E.C. Nista; Marcello Candelli; Filippo Cremonini; Immacolata A. Cazzato; S. Di Caro; Maurizio Gabrielli; Luca Santarelli; M.A. Zocco; Veronica Ojetti; Emilia Carloni; Giovanni Cammarota; Giovanni Gasbarrini; Antonio Gasbarrini
Background : Levofloxacin has been shown to be effective in Helicobacter pylori eradication. Two 10‐day levofloxacin‐based triple therapies were compared with standard 7‐ and 14‐day quadruple regimens in second‐line treatment.
Alimentary Pharmacology & Therapeutics | 2007
Emidio Scarpellini; Maurizio Gabrielli; Lauritano C; Andrea Lupascu; Giuseppe Merra; Giovanni Cammarota; Immacolata A. Cazzato; Giovanni Gasbarrini; Antonio Gasbarrini
Rifaximin is a broad spectrum non‐absorbable antibiotic used for treatment of small intestinal bacterial overgrowth. Doses of 1200 mg/day showed a decontamination rate of 60% with low side‐effects incidence.
Alimentary Pharmacology & Therapeutics | 2005
E.C. Nista; Marcello Candelli; M.A. Zocco; Immacolata A. Cazzato; F. Cremonini; Veronica Ojetti; M. Santoro; R. Finizio; Giulia Pignataro; Giovanni Cammarota; G. Gasbarrini; Antonio Gasbarrini
Background : Standard anti‐Helicobacter pylori therapy may not achieve a satisfactory eradication rate. Fluoroquinolones, such as moxifloxacin, are safe and promising agents for H. pylori eradication.
Helicobacter | 2004
Francesco Franceschi; Maria Antonia Satta; Maria Chiara Mentella; Rebecca L. Penland; Marcello Candelli; R. Grillo; Diego Leo; Lucia Fini; E.C. Nista; Immacolata A. Cazzato; Andrea Lupascu; Paolo Pola; Alfredo Pontecorvi; Giovanni Gasbarrini; Roberto Maria Genta; Antonio Gasbarrini
Recent studies have suggested a role for some infectious agents, including Cytotoxin-associated gene A (CagA)-positive strains of H. pylori, in the pathogenesis of Hashimoto’s thyroiditis (HT), an autoimmune disorder of the thyroid gland defined by the detection of antibodies against thyroglobulin (anti-Tg) and thyroperoxidase (anti-TPO) [1–5]. To verify the possible role of H. pylori in HT we have designed a pilot study with two complementary aims: 1, to compare the prevalence of H. pylori infection (with Cag-positive and -negative strains) in patients with HT and in subject with no evidence of thyroid disease; and 2, to explore the possibility of a molecular mimicry between either anti-Tg or anti-TPO antibodies and any antigenic constituent of H. pylori. Sixteen patients (two men and 14 women, mean age 43.6 ± 11 years) with HT were evaluated for H. pylori infection by 13C urea breath test. Sera from all patients were tested for specific anti-CagA immunoglobulin G (IgG) using a commercial enzyme-linked immunosorbent assay (ELISA) (Radim, Pomezia, Italy). A control group of 20 blood donors (two men and 18 women, mean age 44.2 ± 12 years) without HT was also evaluated. Levels of anti-Tg and antiTPO antibodies in equal amounts of serum were evaluated through immunofluorescence either at enrollment or after absorption [6] with CagA-positive and CagA-negative H. pylori strains as well as with other Gram-negative bacteria, such as Campylobacter jejuni, Pseudomonas aeruginosa, Klebsiella spp. and Escherichia coli. Overall, 37.5% of the patients (six of 16; five women and one man; mean age 47 ± 12 years) with HT had H. pylori infection, compared to 35% of the controls (p > .05). Among infected subjects, 50% of the patients and 45% of the controls were infected by CagA-positive strains (p > .05). None of the absorbance tests with any of the bacteria induced significant changes in the levels of either anti-Tg or anti-TPO antibodies in the sera of patients with HT. The similar prevalence of H. pylori-infection (with and without CagA-positive strains) in patients and controls, as well as the lack of effect of the in vitro absorbance test on the relevant serum antibody titers, indicates that, in contrast to previous observations, an association between H. pylori infection and HT is unlikely. To further explore this relationship, we are currently conducting a clinical trial based on the evaluation of anti-Tg and anti-TPO antibody titers before and after eradication of H. pylori. Another area that may deserve further investigation is the possible cross-reactivity between anti-CagA antibodies and thyroid antigens other than TPO and Tg.
International Journal of Immunopathology and Pharmacology | 2011
Immacolata A. Cazzato; Elisa Vadrucci; Giovanni Cammarota; M. Minelli; Antonio Gasbarrini
Some patients affected by nickel-contact allergy present digestive symptoms in addition to systemic cutaneous manifestations, falling under the condition known as Systemic Nickel Allergy Syndrome (SNAS). A nickel-related pro-inflammatory status has been documented at intestinal mucosal level. The aim of the present study is to evaluate the prevalence of lactose intolerance in patients affected by SNAS compared to a healthy population. Consecutive patients affected by SNAS referring to our departments were enrolled. The control population consisted of healthy subjects without gastrointestinal symptoms. All subjects enrolled underwent lactose breath test under standard conditions. One hundred and seventy-eight SNAS patients and 60 healthy controls were enrolled. Positivity of lactose breath test occurred in 74.7% of the SNAS group compared to 6.6% of the control group. Lactose intolerance is highly prevalent in our series of patients affected by SNAS. Based on our preliminary results, we can hypothesize that in SNAS patients, the Nickel-induced pro-inflammatory status could temporarily impair the brush border enzymatic functions, resulting in hypolactasia. Further trials evaluating the effect of a nickel-low diet regimen on lactase activity, histological features and immunological pattern are needed.
Alimentary Pharmacology & Therapeutics | 2003
Marcello Candelli; Immacolata A. Cazzato; E.C. Nista; Giulia Pignataro; Antonio Gasbarrini
Sirs, Although it was not mentioned by Siproudhis et al., similar results have been obtained previously when chronic anal fissure was treated with glyceryl trinitrate ointment and placebo. These results were based on a much larger group (119 patients) than that described by Siproudhis et al. Usually, such a high rate of healing of chronic anal fissure or of symptomatic improvement, as presented by both groups of authors, is not observed in the placebo group (British Medical Journal Online, in response to the Editorial in the British Medical Journal 2003; 327: 354–5). Siproudhis et al. did not account for this fact in their Discussion, although, in the Introduction, they mentioned that chronic anal fissures very rarely heal spontaneously. Random variables may be responsible for this fact. It was not stated in the study whether any of the patients were administered nitric oxide donors or calcium blockers orally, which might have helped to heal fissures in patients in the placebo group. It was not obvious, either, whether patients with symptomatic haemorrhoids were included in the study — this might have influenced the results. Moreover, in the case of small groups of patients, the numbers of patients resistant to botulinum toxin-A (BT-A) have a large influence on the results. A significant rate of subjective improvement in the group of patients treated with placebo could be attributed to the inclusion of laxatives, ointments and suppositories. The authors did not mention this in their Discussion, where they compared their work with that carried out by Maria et al. It is a pity that, in cases in which no positive effects of treatment were observed, the patients were not administered an additional injection of 100 U. As the effects of the toxin last for about 3 months, it could have been established whether the cumulative dose of BT-A in the group previously treated with BT-A had a positive effect on treatment (which could have been expected) and whether the other group, treated with placebo, was equally sensitive to BT-A. We agree with Siproudhis et al. that the dose of Dysport used in their study was equal to the dose of Botox applied by Maria et al. However, it was not stated whether the botulinum treatment in both cases was identical. Siproudhis et al. tried, but did not manage, to dispel the doubts in this respect saying, However, the internal anal sphincter is easy to identify ... , as it is not known how deep the toxin was administered in both studies. In addition, Jost et al., the first to use botulinum toxin in anal fissure treatment, reported that it is very difficult to be sure that the injection has been administered into the internal anal sphincter as it is very thin (although it can be felt during manual examination). The results of the work by Siproudhis et al. should be interpreted as follows: there were no differences found between 100 U of Dysport and placebo with regard to the treatment of chronic anal fissure. It cannot be stated, however, whether such a result exists because of the size of the population examined, although the authors stated that, we did not observe any trend, whatever variable was considered, towards significant results . My research group has observed that the administration of higher doses of BT-A can improve the results of chronic anal fissure treatment. Brisinda et al. also reported that ...higher doses led to a higher success rate . They observed 96% anal fissure healing after the application of 35 U of Botox (1 labelled unit of Botox is equivalent to 3–6 labelled units of Dysport). The title Lack of efficacy of botulinum toxin in chronic anal fissure , with no doses mentioned, is misleading. We must remember that the results of BT-A treatment depend on the toxin dose.
Gastroenterology | 2010
A.C. Piscaglia; Federico Barbaro; Immacolata A. Cazzato; Luca Di Maurizio; Gianluca Ianiro; Rossella Lamura; Mariachiara Campanale; Giuseppina Bonanno; Sergio Rutella; Tonia Cenci; Luigi Maria Larocca; Giovanni Gasbarrini; Giovanni Cammarota; Antonio Gasbarrini
Purpose: Celiac crisis is a life-threatening syndrome where celiac disease presents with profuse diarrhea and severe metabolic disturbances. Celiac crisis in adults is believed to be uncommon and is not well documented. However, it is likely that many patients with celiac crisis are not definitively diagnosed. In order to improve awareness and to facilitate diagnosis, we reviewed cases of celiac crisis seen at Beth Israel Deaconess Medical Center in Boston, MA and Mayo Clinic in Rochester, MN. These data were used to identify presenting features, formulate diagnostic criteria for celiac crisis in adults and develop treatment strategies. Methods: We reviewed cases of biopsy proven celiac disease in the last 5 years. Celiac crisis was defined as acute onset or rapid progression of gastrointestinal symptoms attributable to celiac disease requiring hospitalization and/or parenteral nutrition along with at least 2 of the 7 factors listed below: 1.Signs of severe dehydration including hemodynamic instability or orthostasis 2.Neurologic dysfunction 3.Renal dysfunction: creatinine >2.0 4.Metabolic acidosis: pH 10 lbs Results: Twelve patients met the above criteria. Of these, 8 were women and 4 were men. 11 developed celiac crisis prior to diagnosis of celiac disease. IgA tissue transglutaminase titer was available for 11 patients. Of these, one had IgA deficiency, and all of the others had elevated tTG, eight with levels greater than 4 times the normal limits. Biopsies of the duodenum in all patients were consistent with a Marsh 3 score. HLA type was available for 10, of which 9 were positive for DQ2 and 1 for DQ8. Patients presented with severe dehydration, renal dysfunction, and electrolyte disturbances, of which hypocalemia was most common. All patients required hospitalization and intravenous fluids and five required parenteral nutrition. Six patients required corticosteroids. All patients had a rapid clinical response to gluten free diet. Conclusion: Celiac crisis is associated with high morbidity and although rarely described, does occur in adults, often without a clear precipitating factor. Patients presentingwith severe unexplained diarrhea and malabsorption should be tested for celiac disease and treatment with systemic steroids or oral budesonide considered. Nutritional support is often required in the short term but most patients ultimately respond to gluten avoidance. We are hopeful that our delineation of formal diagnostic criteria for celiac crisis will aid in identification and management of these patients.
Digestive and Liver Disease | 2007
Immacolata A. Cazzato; Giovanni Cammarota; E.C. Nista; Paola Cesaro; L. Sparano; Valter Giuseppe Bonomo; Giovanni Gasbarrini; Antonio Gasbarrini